A brief overview of Cardiac Auscultation followed by a description of the origin of various sounds produced by the heart from a bio-mechanical perspective

1. Cardiac Auscultation
By William Leach
History
“In 1816, I was consulted by a young woman laboring under general symptoms
of diseased heart, and in whose case percussion and the application of the hand
were of little avail on account of the great degree of fatness. The other method
just mentioned [direct auscultation] being rendered inadmissible by the age and
sex of the patient, I happened to recollect a simple and well-known fact in
acoustics, ... the great distinctness with which we hear the scratch of a pin at
one end of a piece of wood on applying our ear to the other. Immediately, on
this suggestion, I rolled a quire of paper into a kind of cylinder and applied one
end of it to the region of the heart and the other to my ear, and was not a little
surprised and pleased to find that I could thereby perceive the action of the
heart in a manner much more clear and distinct than I had ever been able to do
by the immediate application of my ear.[1]” This is a quote by the French doctor
René-Théophile-Hyacinthe Laennec from 1816 publishing of A Treatise on the
Diseases of the Chest, and on Mediate Auscultation, and it was then that
Laennec invented the stethoscope.
Shortly after in the 1850s, the stethoscope had become one of the doctor’s
vital tools. Learning to listen and diagnose the sounds from the chest became
an important part of a doctor’s training. Yet it wasn’t until the 1890’s that
the wooden stethoscope was replaced by the rubber (and now plastic) much
like the modern stethoscope used today. [2, 3]
Yet there were great men before him that wrote about the sounds produced
by the heart and their correlation to cardiac disease. Hippocrates (460 – 370
BC), stressing the diagnostic value of auscultation wrote “You shall
know by this that the chest contains water but not pus, if in
applying the ear during a certain time on the side, you perceive a
noise like that of boiling vinegar.” And then it was not until 1628
that WilliamHarvey picked up where Hippocrates left off. In his
publication of On the Motion of the Heart and Blood (translated
from De Motu Cordis), Harvey’s treatise provided the first
description of heart sounds when he stated “So it is with each
movement of the heart when a portion of the blood is transferred
from the veins to the arteries, that a pulse is made which may be
heard within the chest. . . (and I describe the sound) as . . . two
clacks of a water bellows to raise water.” [2, 3]
Drawings of the early
stethoscope by Rene
Theophile Hyacinthe
Laënnec, 1819 [1]
History of the Stethoscope 4

2. Prior to the invention of the stethoscope physicians of their time auscultated the heart but with
little efficiency as they only were able to do so via direct auscultation, or pressing the ear against
the chest. Since Laennec invented his heart listening device there has been tremendous
advancement in various methods now used to diagnose cardiac pathologies. [2]
Acoustics
The Stethoscope
The word “stethoscope” is derived from the Greek words stethos = breast and skopein = to explore.
Sound is heard via frequency and pitch. Frequency refers to the number of oscillations per second
made by a sound-producing structure, while pitch is what you hear when those vibrations act on
your hearing apparatus. As far as membranes go, the tauter the membrane the higher it’s natural
frequency of oscillation and the more efficient it is at higher frequencies. The bell does not have an
artificial diaphragm and therefore uses the patient’s loose skin as its diaphragm, and thus the bell is
more efficient at hearing lower frequencies. On the other hand, the diaphragm contains an artificial
smooth, stiff diaphragm, and thus is better at hearing higher frequencies. Although it is not just
that simple. Cardiac sounds do extend much over 1,000 cps (17 Hz), which is considered a low
frequency. Therefore the bell can actually hear both the lower and higher frequencies produced by
the heart. Lower frequencies are also know to dampen higher frequencies and interfere with
isolating the higher frequency sounds. The taught diaphragm acts to filter out the lower
frequencies so the higher frequencies can be heard with less interference. Adults can hear
frequencies of up to 14,000 (230 Hz) cycles per second (cps). Typical hearing loss in older physicians
usually spares frequencies below 3,000 cps (50 Hz). Therefore natural hearing loss should not
interfere with the ability to hear cardiac sounds. [4, 5]
Sounds Produced in the Heart
Sounds in the heart are produced abrupt changes in the velocity
of the bloodstream. These changes in velocity are affected by
the interplay of the dynamic events associated with the
contraction and relaxation of the atria and ventricles, the valve
movements, and blood flow. The change in velocity creates
turbulence in the blood which produces vibrations in the cardiac
tissues that can be sensed by the human ear as sound. The more
abrupt the change in velocity, the higher the frequency of vibrations,
and thus the higher the pitch. These discrete bursts of auditory
vibrations can be described by intensity (loudness), frequency (pitch),
quality and duration. [5, 6]
The attenuation of the vibrations is the least in the blood when
compared to other cardiac anatomical structures. There are different
areas on the surface of the body over the cardiac region where
attenuation of the sound producing vibrations are at their least and
intensity is at its greatest depending on the origin, surrounding
[6]
[6]

3. tissues, and vector of the turbulence produced. Thus these areas are where sounds may be best
heard. The five classic listening areas are the:
Aortic Area – right 2nd intercostal space at the sternal border
Pulmonic Area – left 2nd intercostal space at the sternal border
Erb’s Point – left 3rd intercostal space at the sternal border
Tricuspid Area – 5th intercostal space parasternally
Mitral Area – left 5th intercostal space at the mid-clavicular line
Normal Heart Sounds
Normal physiology of the heart produces an organized and
sequential set of sounds, or abrupt changes in blood flow
velocity, which have been identified as S1, S2, S3, and S4.
S1
The first heart sound is caused by the closure of the mitral and
tricuspid valves, and coincides with the contraction of the ventricles, thus identifying the onset of
systole and the end of diastole. Normally the closure of the mitral valve (M1) precedes the closure
of the tricuspid valve (T1) by 20 – 30 msec. The source of the sound is not caused by the actual
contact of the valve cusps. Rather, after the AV valves close they are stretched toward the atrium
by the momentum of the ventricular blood mass. As counter-acting elastic forces of the
components of the AV valves equal the force exerted from the ventricular blood, a stretch-recoil
mechanism occurs causing vibrations in the blood mass as well as the heart tissues. The anatomical
position of the AV valves, particularly the mitral valve, along with the recoil vector produced, as well
as the location of the largest volume of blood cause the greatest intensity of vibrations at the apex
of the heart. Thus S1 is the loudest at the mitral area although an audible sound is heard in each of
the four classic listening areas. The intensity of S1 is largely determined by M1. Pathologies causing
an electrical delay in activation of the two ventricles, such as a right bundle branch block or
Ebstein’s anomaly, can increase the time between M1 and T1 to 60 msec. [5, 6, 7]
S2
The second heart sound is caused by the closure of the aortic and pulmonic valves, and coincides
with the incisurae (dicrotic notch) of the aorta and pulmonary pressure curves and terminate left
and right ventricular ejection periods. It has a shorter duration and higher frequency than S1. The
diaphragm portion of the stethoscope is best for identifying a split S2 since these are of higher
frequency than S1 and therefore the diaphragm will filter out the lower frequency sounds produced
by S1. In a normal healthy heart the closure of the aortic valve (A2) precedes the closure of the
pulmonic valve (P2) by 2 to 8 msec. since right ventricular ejection begins prior to left ventricular
ejection, has a slightly longer duration, and terminates after left ventricular ejection. Similarly to S1
the source of the sound is not caused by the contact of the cusps. Rather the sound producing
vibrations are a result of sudden deceleration of retrograde flow of the columns of blood in the
aorta and pulmonary artery. This sudden deceleration occurs via the same stretch-recoil
mechanism as in S1 creating after-vibrations in the cusps, walls and blood columns of the great
vessels, and their respective ventricles. The greatest vector of these oscillations follows the same
principles as S1 and therefor is located along the path of the great vessels which are located in the
[5]

4. aortic and pulmonic listening (also Erb’s point) areas respectively, although the sounds are also
audible in each of the five classic listening areas. [5, 6, 7]
A2 and P2 may be heard as two distinct sounds, which is known as splitting, and occurs both
normally (physiologically) and pathologically. In order for a human to differentiate the two they
must be separated by more than 20 msec. Traditionally it was believed that an inspiratory drop in
intrathoracic pressure favored greater venous return to the right ventricle, pooling of blood in the
lungs, and decreased return to the left ventricle. The increase in right ventricular volume prolonged
right-sided ejection time and delayed P2 while the decrease in left ventricular volume reduced left-
sided ejection time and caused A2 to occur earlier. However, the delayed P2 and early A2 associated
with inspiration are actually correlated with the interplay between changes in the pulmonary
vascular impedance and changes in systemic and pulmonary venous return. In a normal physiologic
setting, inspiration lowers impedance in the pulmonary circuit, prolongs the hangout interval and
delays pulmonic valve closure, resulting in audible splitting of A2 and P2. On expiration, the reverse
occurs: pulmonic valve closure is earlier and interval is separated by less than 30 msec. causing S2 to
be heard as a single sound. Since the pulmonary circulation has a much lower impedance than the
systemic circulation, flow through the pulmonic valve takes longer than flow through the aortic
valve. The inspiratory split widens mainly because of delay in the pulmonic component. In children,
teens, and young adults increasing intrathoracic pressure can cause audible splitting of S2. This can
be achieved simply by the Valsalva maneuver or even simply by squatting. [5, 6, 7]
Splitting of S2 may also be secondary to pathologies affecting the heart. This is determined when
the split is audible during both inspiration and expiration, otherwise known as a Persistent S2 split.
A right bundle branch block is the most common pathological cause of persistent auditory S2 split,
but may occur with other conditions causing delayed electrical activation of the right ventricle such
as Wolff-Parkinson-White syndrome. Additionally, pathologies causing decreased impedance of the
pulmonary vascular bed may be the cause, such as an atrial septal defect. Furthermore, anything
which may cause right ventricular pressure overload, such as pulmonary hypertension with right
sided heart failure, may cause the S2 split. Paradoxical (reversed) splitting is due to conditions
causing left prolonged left ventricular activation or emptying such as a left bundle branch block. [5, 6]
S3
There are two phases of diastolic filling: the rapid filling phase which occurs passively upon opening
of the AV valves, and the atrial contraction phase which occurs actively in late ventricular filling.
The third heart sound is caused by the former producing a brief, low frequency vibration occurring
in the right or left ventricle. During ventricular contraction, the mitral and tricuspid valves are
closed, and atrial pressure rises from the influx of blood into the atria. When ventricular pressure
falls below atrial pressure in early diastole, the AV valves open widely and the blood from the atria
rapidly drains into the ventricles. The ventricular walls become distended and when the opposing
elastic forces created by the ventricular tissue reach the force acting on the wall from the pressure
of the increased volume of blood, the diastolic inflow of blood is suddenly decelerated causing
vibrations to be sent throughout the ventricular blood mass. Therefore, the sound is heard best
over the ventricles, particularly at the apex of the heart or the mitral area. The sound is difficult to
hear since the usual frequency is near the lower limit of human hearing (25-50 Hz). [5, 6, 7]

5. This sound is normal in children and adults up to 40 year old. In patients over 40, the presence of
an audible S3 is an indication of a significant increase in the volume load on the ventricle(s), with
heart failure being the most common cause. Factors that seemto relate to the presence and
intensity of the third heart sound include age, atrial pressure, unimpeded flow across the
atrioventricular valve, rate of early diastolic relaxation and elasticity of the ventricle, blood volume,
ventricular cavity size, diastolic momentum of the heart, degree of contact with the chest wall,
thickness and character of the chest wall, and the position of the patient. Since this sound is of very
low frequency, it is almost exclusively heard with the bell portion of the stethoscope. Additionally,
since the intensity is also very low and the sound does not widely radiate, it can be better heard in
the Decubitus position which bring the apex of the heart closer to the chest wall ultimately
decreasing the attenuation of the sound producing vibrations. [5, 6]
Synonymous terms include ventricular gallop, early diastolic gallop, ventricular filling sound, and
protodiastolic gallop. The term gallop was first used in 1847 by Jean Baptiste Bouillard, and perhaps
the best description was provided by a pupil of Bouillard’s, Pierre Carl Potain, who stated “One
distinguishes therein three sounds, namely: two normal sounds of the heart and a superadded sound
. . . . This sound is dull, much more so than the normal sound. It is a shock, a perceptible elevation; it
is hardly a sound. If one applies the ear to the chest it is affected by a tactile sensation, perhaps
more so than an auditory one. . . . In addition to the two normal sounds, this bruit completes the
triple rhythm of the heart. It thus produces a rhythm of three sounds unequally distinct, and
occasionally unequally distant, a rhythm which the ear seizes with extreme facility, provided that it
had once perceived it distinctly. This is the bruit de galop.” [6]
S4
The sound produced by S4 is the result of late ventricular filling. During late diastole the atria
contracts in order to empty the remaining blood into the ventricle, known as the “atrial kick”. This
contraction is required to overcome the building pressure in the ventricle due to increasing blood
volume causing increased opposing elastic forces of the ventricular wall. The sound producing
mechanism is the same as S3. This sound is also similar in frequency as S3 (20 – 30 Hz). The main
difference is the timing of which the sounds are heard. S3 occurs in early diastole, or just after S2,
and S4 occurs in late diastole, or just prior to S1. Decreased ventricular compliance with increase the
intensity of S4. This may result from left ventricular hypertrophy secondary to systemic
hypertension, or reduced right ventricle compliance secondary to pulmonary hypertension. S4 is
considered normal in patients over 50 due to decreased compliance due to aging. However, the
presence of S4 does not always indicate decreased compliance and can occur secondarily to other
pathologies. The presence of both S3 and S4 is known as a summation gallop and is indicative of
atrial fibrillation. [5, 6]

6. Murmurs
Murmurs are created by disturbance of laminar blood flow (i.e., turbulence), but turbulence per se
does not produce adequate acoustic force to be audible at the chest wall. The most widely accepted
theory concerning the generation of murmurs was popularized by Bruns and incorporates the
concept of vortex shedding. Vortices are tiny eddies created by an obstruction to the laminar flow of
blood. The concept of vortex shedding can be simplified by employing a familiar analogy-a boulder
protruding through the surface of a fast-moving stream. The undisturbed water flows without
interruption until it hits the boulder. The boulder causes the stream to separate and generate
vortices, or tiny eddies that move in a spiral fashion and are shed in the general direction of the flow
of the stream. As the vortices are she they leave in their place wakes, which are areas of relatively
"still water." Water rapidly moves in to fill the wakes left by vortex shedding. The sound that one
hears when water is rushing around the boulder is generated by the filling of wakes left by the
shedding of vortices. In the cardiovascular system, deformities of valvular structures and
discontinuity in the walls of the heart or great vessels produce vortex shedding. Velocity plays a
major role in the amount of vortex shedding that takes place. The higher the velocity of the blood
flow, the higher the frequency of vortex shedding. [6]
Systolic murmurs are best classified with time of onset and termination while diastolic murmurs are
best classified according to time of onset only. [7]
Diastolic Murmurs
A diastolicmurmurisa soundof some durationoccurringduringdiastole.All diastolicmurmursimplysome
alterationof anatomyor functionof the cardiovascularstructures.The fourmostcommonlyencountered
diastolicmurmursinclude aorticandpulmonaryvalveregurgitation,andmitral andtricuspidvalve rumbles.
Comparedtomost systolicmurmurs,diastolicmurmursare usuallymore difficulttohear,andcertain
techniquesare essential fortheirdetection. Diastolicmurmursare longer
indurationsince the diastolicphase islongerindurationthatthe systolic
phase.
Aortic Regurgitation
Aorticvalve regurgitationisthe lossof perfectappositionof the aortic
cuspsin diastole usuallyasa resultof the deformityof the cuspsor
supportingstructures. Whenthe valvesare open,the bloodflow islaminar
and vortices are not significantly created. However,whenthe deformed
valvesclose theydonotpreventthe backflow of bloodintothe left
ventricle. Asthe flowpassesoverthe deformedcuspsitcreates vorticesin
the back flowintothe leftventricle. Therefore the soundisheardbest
immediatelyafterthe bloodflowsbackoverthe cups,whichisat Erb’s
point. The pressure gradientishigh,causingahighervelocityof blood
flow,thuscreatinga higherfrequencysound. [6]
[7]

7. Mitral Stenosis
The stenosisof the mitral valve isusuallyassociatedwithpreviousrhurmaticfeverthatcausesscarformation
and fusioncommissures. Thiscausesthe valve toopenmore quicklyandproduce a“snap” or a brief intense
turbulence. Since the pressuregradientacrossthe mitral valve increases,the intensityof the sound
producedincreases. Asmentionedinthe mechanismsforS3and S4, there are two phasesof ventricular
filling. Thereforethe pressure gradient(intensity) isgreatestduringmid-diastolicfillingandanotherburstof
intensityjustafterthe “atrial kick”. Asthe turbulence isproducedfromthe bloodflowingacrossthe cusps,
the soundswill be bestheardjustafterthe bloodflowsoverthe cusps,orin the mitral area. [5, 6, 7]
Systolic Murmurs
A murmur is a series of vibrations of variable duration which emanate from the heart or great
vessels. A systolic murmur is a murmur that begins during or after the first heart sound and ends
before or during the second heart sound. There is a grading systemassociated with the intensity of
systolic murmurs.
1: Heard with careful listening.
2: Readily audible with stethoscope is applied to the chest.
3: Louder than 2 without a thrill
4: Loud with associated thrill
5: Audible even when only the edge of stethoscope touches the chest
6: Audible without a stethoscope.
Aortic Stenosis
Sounds produced by aortic stenosis follow the same mechanism as mitral stenosis. However the
pressure gradient is much greater and thus velocity across the leaflet is greater, thus the frequency
of the sound produced is higher. The vortices are created as the blood flow passes the stenotic
valves and therefore the sound is heard best over Erb’s point and the aortic area. [5, 6, 7]
Mitral Regurgitation
Sounds produced by mitral valve regurgitation also follow the same mechanism as aortic
regurgitation. The pressure gradient is also high, producing a high frequency sound again. As the
flow is from the left ventricle to the left atrium, the vortices are produced as the blood flows across
the cusps and thus the sound is best heard toward the base of the heard, in the pulmonic area. [5, 6, 7]

8. References
1. Laennec,R.T.H. De l’Auscultation Médiateou Traité du DiagnosticdesMaladiesdes Poumonsetdu
Coeur.Paris:Brosson& Chaudé, 1819.
2. Silverman,MarkE. "De Motu Cordis:The LumleianLecture of 1616: An ImaginedPlayletConcerning
the Discoveryof the Circulationof the BloodbyWilliamHarvey." Journalof theRoyalSociety of
Medicine 100.4 (2007): 199-204.
3. Hanna, IbrahimR.and Mark E. Silverman."A Historyof CardicaAuscultationandSome of Its
Contributors."TheAmerican Journalof Cardiology (2002):259-267.
4. Welsby,P.D.,G. Parry and D. Smith."The stethoscope:some preliminaryinvestigations." Postgrad
Med J 79 (2003): 695–698.
5. Constant,JulesM.D.F.A.C.C. Essentialsof BedsideCardiology.2nd.Totowa,N.J.:Humana,2003.
6. Felner,J.M. Clinical Methods:TheHistory, Physical,and Laboratory Examinations.3rd.Boston:
Butterworths,1990.
7. Netter,F.H. The Netter Collection of MedicalIllustrations:The CardiovascularSystem.2nd.Vol.8.
Philadelpha,PA:ElsevierSaunders,2014.